Ophthalmologic Manifestations of Botulism Clinical Presentation

Updated: May 19, 2016
  • Author: Bhupendra C K Patel, MD, FRCS; Chief Editor: Hampton Roy, Sr, MD  more...
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The diagnosis of botulism requires a high degree of clinical suspicion. Although laboratory confirmation is required, the diagnosis should be suspected on clinical findings, in those patients with an appropriate history and physical (particularly neurologic) examination.

Food poisoning

The severity of illness varies from a mild condition to a very serious disease with death within 24 hours. The incubation period is generally 18-36 hours; however, it may vary from several hours to several days.

The initial symptoms are usually those of motor cranial nerve involvement with onset of diplopia, dysphonia, and dysphagia. A generally symmetric descending paralysis follows. Abdominal pain, with nausea and vomiting may precede or follow paralysis. A dry mouth and throat reflect cholinergic parasympathetic disturbance. Patients generally remain alert and responsive. Sensory deficits, besides blurred vision, have been reported only in rare cases.

Wound infection  [7]

The incubation period averages about 7 days. Wound botulism may occur in any wound contaminated by soil or water.

Symptoms are generally the same as those seen in food-borne botulism, except gastrointestinal symptoms are absent. The source wound may appear relatively benign. Wound infections associated with intravenous drug needle puncture sites are becoming an important cause.

Infant botulism  [8]

The incubation period varies from 3-30 days. In this form of botulism, the severity ranges from mild illness with failure to thrive to severe paralysis with respiratory failure.

Infant botulism causes acute bulbar dysfunction. The first sign of the disease may be constipation. Other features include lethargy, hypotonia with poor head control, poor feeding, with difficulty in sucking and swallowing, and pooled oral secretions. Respiratory failure occurs in up to one half of diagnosed infants.

The identification of contaminated honey as a source of spores has lead to the recommendation that honey should not be given to infants younger than 1 year. Susceptibility decreases with age as the normal intestinal flora develops.



The major systemic features of botulism involve motor weakness or paralysis. Paralysis begins with cranial nerve involvement and progresses caudally to involve extremities.

Clinical physical findings involve the following:

  • Symptoms of motor cranial nerve involvement with onset of dysarthria, dysphonia, and dysphagia may be present.

  • A generally symmetric descending paralysis occurs, with involvement of neck, arms, thorax, and legs.

  • Respiratory difficulties occur with intercostal and diaphragmatic weakness.

  • Autonomic features are to be expected, reflecting cholinergic neurotransmission disruption, with impairment of salivary secretion, paralytic ileus, constipation, and urinary retention.

  • Postural hypotension may be present.

  • The gag reflex may be suppressed.

  • Typically, patients are afebrile.

Ophthalmic manifestations may reflect the anticholinergic effects of the neurotoxins. [9, 10]

  • Accommodation paresis, with blurred vision

  • Pupil dysfunction with mydriasis and poorly reactive pupils

  • Dry eye symptoms with impairment of lacrimation

Ophthalmic manifestations may reflect a deficit at the neuromuscular junction. [11, 12, 9, 10]

  • Oculoparesis or ophthalmoplegia manifests as diplopia.

  • Blepharoptosis is common.

  • Nystagmus may be noted.

Ocular manifestations may be the manifesting features of botulism. However, their absence does not exclude this disease, since the various toxins appear to involve the ocular system to various degrees. Neurotoxin A may have no specific ophthalmic manifestations.

In wound botulism, the symptoms are generally the same as those seen in food-borne botulism, except gastrointestinal symptoms are lacking.

In the infant, the clinical examination may note neurologic features of ptosis, ophthalmoplegia, weak gag reflex, and poorly reactive pupils, in addition to systemic features of generalized muscle weakness with hypotonia and a weak cry.



Botulism is a disease caused by the neurotoxins of C botulinum.